Attention A T users. To access the menus on this page please perform the following steps. 1. Please switch auto forms mode to off. 2. Hit enter to expand a main menu option (Health, Benefits, etc). 3. To enter and activate the submenu links, hit the down arrow. You will now be able to tab or arrow up or down through the submenu options to access/activate the submenu links.

Boise VA Medical Center

 

Research

Basic Science & Clinical Research to Improve the Health and Healthcare of Veterans

Research Mission Statement: Our mission is to continually improve the health of all veterans through basic science discoveries and clinical research studies. Investigators at the Boise VA have contributed to advancements in our understanding of aging, cancer, heart disease, nervous system disorders, lung function, and the pathology and treatment of infectious diseases, including those with antibiotic resistance.  Our clinical trials have yielded new therapies for skin and soft tissue infections, hepatitis C, and chronic wound healing.  We strongly believe that today’s scientific research defines tomorrow’s standard of patient care.

Dennis L. Stevens, M.D., Ph.D.
Associate Chief of Staff for Research

 

Researcher Profiles, Basic Science

Dennis L. Stevens, M.D., Ph.D.

Dr. Stevens is the Chief of Infectious Diseases at the Boise VA Medical Center, Professor of Medicine at University of Washington School of Medicine, and Associate Chief of Staff for Research and Development at the Boise VA. He is a recognized as a world leader in the field of infectious disease pathogenesis.  For the past 35 years, Dr. Stevens has investigated the role of extracellular toxins of gram positive microbes in the pathogenesis of severe infection. His laboratory has success in the identification, isolation and characterization of the mechanisms of action of protein toxins from group A streptococcus, Clostridium perfringens, C. sordellii, C. septicum and Staphylococcus aureus. His lab has also developed recombinant toxins, monoclonal antibodies against these toxins and has generated strains of these pathogens which no longer express these toxins. Dr. Stevens has participated in numerous clinical trials investigating novel treatments for bacterial and viral infections, with findings directly translated into improved patient care for veterans and civilians with these devastating infections.  Dr. Stevens has authored over 170 journal articles, 7 medical reference and textbooks, and over 100 book chapters.

Amy E. Bryant, Ph.D.

Dr. Bryant is a Research Career Scientist at the Boise VA Medical Center, and Associate Professor at University of Washington School of Medicine. For 30 years she has studied the host/pathogen interactions responsible for vascular injury, tissue destruction and multiorgan failure in life-threatening infections including those due to C. perfringens, C. septicum, Streptococcus pyogenes, and methicillin-resistant Staphylococcus aureus. Her laboratory has identified and characterized key bacterial- and host-derived factors involved in pathogenesis and has tested novel strategies for treatment. This research has contributed to the current standard of care for treatment of severe soft tissue infections due to S. pyogenes, S. aureus and C. perfringens. Dr. Bryant’s current research focus is on the mechanisms responsible for cryptic group A streptococcal infections of injured muscle, and the role of NSAIDs in this process. With an overarching goal to improve diagnosis and treatment and reduce the incidence of amputation in these devastating infections, she also seeks novel biomarkers to reveal infection before severe complications develop, and seeks to elucidate the mechanisms in the rapid progression of clostridial myonecrosis.

Michael J. Aldape, Ph.D.

Dr. Aldape is an Associate Research Scientist with the Infectious Diseases Research Group at the Boise VA Medical Center, and Assistant Professor of Biology at Northwest Nazarene University. He is a leading expert in the field of C. sordellii pathogenesis, having been among the first to fully elucidate the mechanisms involved with the high fatality rate of this pathogen. Dr. Aldape’s research on C. difficile has provided support for the discovery that antibiotic use may trigger C. difficile infection by affecting the virulence properties of the micro-organisms involved. Dr. Aldape’s current research focuses on the mechanisms associated with the leukemoid reaction observed in infections caused by Clostridium sordellii and Clostridium difficile, and he has published several journal articles about this work.

Devin D. Bolz, Ph.D.

Dr. Bolz is an Assistant Research Scientist at the Boise VA Medical Center, and Adjunct Professor of Biological Sciences for Boise State University.  He has over ten years of experience investigating the impact of the innate immune response on pathogen burden, development of pathology and host survival during bacterial infection. His current research focuses on defining key molecular events in the pathogenesis of Staphylococcus aureus and other drug-resistant bacterial pathogens, and improving our understanding of how bacteria regulate the expression of virulence factors, including exotoxins. The aim of these studies is to define networks that can be exploited for improved diagnostics and innovative intervention strategies to reduce disease incidence and provide protection against lethal and disabling infections.

Sarah E. Hobdey, Ph.D.

Dr. Hobdey is an Assistant Research Scientist at the Boise VA Medical Center. With a background in protein biochemistry and molecular biology, she has developed expertise in protein expression, purification and structure-function characterization for application to diverse scientific disciplines. Her current research is centered on bacterial toxin production related to current antibiotic treatments. This research explores the possibilities of novel therapies for the treatment of toxic bacterial infections utilizing adaptive immunity-derived neutralizing antibodies in conjunction with traditional antibiotics.

Mary Cloud Ammons, Ph.D.

Dr. Ammons is an Assistant Research Scientist of Infectious Diseases at the Boise VA Medical Center. Dr. Ammons completed her PhD in molecular immunology at Montana State University in 2007 and her post-doctoral work in medical biofilms at Montana State University in 2009. For the past seven years, Dr. Ammons has been an Assistant Research Professor in biochemistry at Montana State University where she played a key role in developing the metabolomics program. Her long-term career objective is to pursue a research program that seeks to solve the many unknowns of the host innate immune cell interaction with opportunistic microbial biofilms. Having completed doctoral studies in regulatory molecular mechanisms of phagocytic cells and postdoctoral studies in developing novel, metabolically-disrupting, biofilm-targeted antimicrobials, she is uniquely positioned to apply metabolomic techniques to elucidate these issues. The complex interaction between host innate immune cells and pathogenic bacterial biofilm in chronic wounds provides an ideal model system for the emergent field of metabolomics as there are significant gaps in basic research to explore as well as ample opportunities for innovative translational research such as the development of novel therapeutics and diagnostics. Working with the Boise VA Medical Center, Dr. Ammons’ research specifically targets development of better treatment protocols to promote healing in the chronic wounds afflicting our Veteran population and she hopes to bring a better quality of life to our wounded warriors and their families.

Jay R. Radke, Ph.D.

Research in my laboratory is focused on understanding how two human adenovirus (Ad) genes (E1A and E1B) modulate both the host innate immune response and cell death pathways. The ultimate goal of our research is to develop novel treatments for virus induced acute respiratory distress syndrome (ARDS) and for improving the efficacy of oncolytic adenoviruses for treating cancer. We have described a novel, immunorepressive activity of Ad infected dying cells (termed Ad CPE corpses) that modulate the Ad-induced, innate immune response. Ad CPE corpse repression of macrophage-mediated inflammatory responses requires expression of the Ad protein, E1B 19/20K. Ad CPE corpses resulting from infection with Ad that lack E1B 19K, fail to repress Ad-induced macrophage pro-inflammatory responses and, in contrast, can induce increases in such responses. Ad14p1 is an emergent strain of Ad14 that induces a strong inflammatory response during infection that can result in severe, acute lung injury and, in some cases, ARDS. Studies showed reduced E1B 20K expression in virally infected human cells, when compared with wild type (wt) Ad14 infection. As a result, Ad14p1 CPE corpses fail to repress pro-inflammatory macrophage responses, whereas wt Ad14 CPE corpses are markedly immunorepressive. Syrian hamsters are permissive for human adenoviruses. Infection of Syrian hamsters revealed that Ad14p1 infection induces a patchy bronchopneumonia that is not seen following infection with Ad14. Ad14p1 infected hamsters also show up-regulation of pro-inflammatory cytokines, consistent with our in vitro model system. Currently, we are developing new methods to characterize the innate immune response in the lungs of Ad14p1 lungs and testing novel mechanisms through which Ad14 CPE corpses repress pro-inflammatory macrophage responses. With the goal to developing novel methods to treat viral and non-viral induced ARDS. The second focus of my research is understanding how stable expression of E1A (outside the context of viral infection) alters cellular apoptotic pathways, which results in cellular sensitivity to both innate immune effector cells, chemotherapeutic drugs and other apoptosis inducing agents as well as to innate immune effector cells such as activated macrophages and natural killer cells. We have demonstrated that E1A sensitizes cells to apoptosis induced by intrinsic injuries by enhancing caspase-2 activation through the PIDDosome. It appears that PIDDosome mediated caspase-2 activation is also required for macrophage and NK induced cell death of E1A expressing cells. We are currently trying to identify how E1A expression regulates PIDDosome formation and its activation of caspase-2.

Researcher Profiles, Clinical Research

Margaret Doucette, D.O.

Dr. Doucette is Chief of Physical Medicine and Rehabilitation at the Boise VA Medical Center.  Because a large percentage of the hospital patient population is diabetic, Dr. Doucette remains on the cutting edge of wound treatment and pressure ulcer innovations.  She recently wrote an article on the use of new wireless technologies to improve patient turning compliance and reduce incidence of pressure ulcers.  Dr. Doucette’s current clinical research explores the use of amniotic tissue patches as a therapy for chronic wound healing in patients at high risk for amputation. 


Idaho Veterans Research and Education Foundation (IVREF)

The Boise VA Medical Center, Research Department is also affiliated with the Idaho Veterans Research and Education Foundation. To learn more about the IVREF go to their website by clicking here.

Contact Info

Location

  • Boise VAMC
    Bldg. 117

Contact Number(s)

  • 208-422-1000

Hours of Operation

  • 8am to 4:30pm